Persistent foot ulcer due to ruxolitinib therapy for primary myelofibrosis.

Primary myelofibrosis is characterized by bone marrow fibrosis, splenomegaly and presence of JAK-2 V617F mutation in more than 90% of patients. Ruxolitinib is a Janus kinase inhibitor used for the treatment of primary myelofibrosis. We describe herein a persistent foot ulcer development attributed to ruxolitinib therapy. We are unaware of any previous reports of this phenomenon in the scientific literature. A thorough examination of the lower extremities is perhaps necessary before initiating this oral agent. If ruxolitinib therapy cannot be safely discontinued, diligent wound care and a course of antibiotics are warranted.

Lacking the 'protective label' of diabetes: Phenytoin-induced distal symmetrical peripheral neuropathy. A clinical case report.

This report documents an unusual case of distal symmetrical peripheral neuropathy (DSPN) in an otherwise healthy patient without diabetes mellitus (DM) presenting to a podiatric wound care clinic. The development of gas gangrene coupled with Charcot neuroarthropathic changes ultimately resulted in a potentially life-saving transmetatarsal (TMT) amputation. Causation of, or at least a contributor to, the DSPN was likely phenytoin usage for epileptic seizures. Long-term use of phenytoin can lead to axonal shrinkage and random clusters of nerve demyelination [1]. Clinical standards for DM-induced DSPN indicate that annual comprehensive neurological assessment to detect nerve function deterioration is warranted [2]. This can aid in identifying patients at high risk of diabetic foot ulceration. However, oftentimes, patients exhibiting medication-induced neuropathy are not assessed to determine severity of the neuropathy nor are they educated about ulcer prevention in the same manner as patients with DM. This report advocates for a standardized threshold of diagnostic and preventative investigation for neuropathy of all aetiologies; diabetic, traumatic, viral, medication-induced and idiopathic.

Acute dermal and inhalation exposure to 4-vinylpyridine--a case report.

INTRODUCTION: To the best of our knowledge there are only few reports in medical literature concerning the acute dermal exposure to 4-Vinylpyridine (4-VP). We describe a dermal and inhalation exposure to 4-VP followed by systemic symptoms and local injury. CASE REPORT: A 58-year old female, with non significant previous medical history, was admitted to the ward with the signs of vertigo, weakness and local pain in the foot dorsal region after exposition to few drops of 4-VP. After 7 days of the treatment all symptoms resolved. CONCLUSION: Vinylpyridines are irritant and corrosive substances which can lead to skin damage. In case of inhalation exposure the late onset of systemic symptoms should be taken into account.

Hydroxyurea-induced foot ulcer in a case of essential thrombocythaemia.

OBJECTIVE: To illustrate the association between hydroxyurea and the development of ulcers. METHOD: A case study is presented, in which histological changes, mean corpuscular volume (MCV) and transcutaneous oxygen tension (TcPO2) were all measured and analysed, both during hydroxyurea treatment and following it's discontinuation. RESULTS: Two months following the cessation of hydroxyurea therapy, the patient's ulcer had healed completely. Biopsy specimens taken before and after its discontinuation showed a considerable improvement in vascularity, with a capillary density 6.28 times higher after discontinuation of the drug. TcPO2 was just 8mmHg at the first measurement, and this increased to 65mmHg at the second. CONCLUSION: These findings suggest deficient neovascularisation and circulation during hydroxyurea treatment. Changes in MCV also appeared to have an effect on the progress of wound healing, which supports the hypothesis that macroerythrocytosis may be involved in the development of these rare ulcers, via impairment of the microcirculatory rheology.

Pedal neuroarthropathy in a nondiabetic patient as a result of long-term amiodarone use.

UNLABELLED: In this article, we describe a case of a man without diabetes with a long history of amiodarone use. He presented with a foot deformity and plantar ulceration. Examination showed him to have a symmetrical peripheral neuropathy and findings consistent with a Charcot foot. Extensive investigations failed to find other causes for his neuropathy, other than his amiodarone use. We believe that this is the first reported case of a neuropathic foot deformity and ulceration occurring with amiodarone use, and we feel that it is important to point out the association of this commonly used antiarrythmic drug with this form of neuropathic osteoarthropathy. LEVEL OF CLINICAL EVIDENCE: 4.

Soft tissue necrosis following using calcium phosphate cement in calcaneal bone cyst: case report.

Calcium phosphate cements have received widespread attention for their possible role as bone-grafting material and bone fillers in skeletal defects. They were evaluated as a biomaterial in many aspects. No serious harmful effects such as foreign body reaction and tissue necrosis against to calcium phosphate cements have been reported yet. They were accepted as highly biocompatible materials. In this paper, we represent a patient who had soft tissue necrosis around lateral malleolar region, following using percutaneous calcium phosphate cement as a filler bone substitute in calcaneus bone cyst. The possible mechanisms were discussed.

Painful ANA-positive scleroderma-like disease with acral ulcerations: a case of chronic gangrenous ergotism.

Chronic ergotism is a rare cause of limb ischemia. In this case report, the authors present a 62-year-old woman with history of long-term use of ergotamine alkaloids for the treatment of menstrual pain, who developed a severe painful disease initially misdiagnosed as systemic sclerosis (scleroderma) for 3 decades. She presented with a combination of acral gangrene, foot ulcer, renal obstruction, mild pulmonary fibrosis, and reduced esophageal motility. Right-sided renal obstruction was evident. The condition was extremely painful and had led to muscular contractions and immobility, drug abuse, and anemia. After establishing the diagnosis of chronic gangrenous ergotism, changing drug therapy, mobilization, and treatment of chronic wounds, she showed a remarkable recovery. Eventually the foot ulcer was closed successfully using a mesh graft transplantation, and the patient was able to walk alone. Chronic ergotism is rare but has to be taken into account when presented with painful chronic digital and foot ulcers.

Vascular events associated with alpha interferon therapy.

Alpha Interferon (IFN) is a biological agent used for the therapy of an increasing number of diseases, either as an established effective therapeutic tool or in the context of clinical trials. The use of IFN may be complicated by serious adverse reactions. We describe here the clinical course of a variety of vasculopathic complications in association with IFN-therapy in 12 patients with the diagnosis of chronic myeloid leukemia and 1 patient with malignant melanoma treated at our institute. Vascular manifestations in these patients include Raynaud's phenomena, digital ulcerations and gangrene, pulmonary vasculitis, pulmonary hypertension and thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS). These reactions occurred after 3 months to 3 years of 3-10 million units (MU) daily IFN therapy. Concomitant administration of hydroxyurea (HU) was noted in 5 patients. Discontinuation of IFN and initiation of immunosuppressive therapy brought about a complete resolution or arrested progression of these reactions. IFN-therapy may be complicated by severe vasculopathic/vasospastic complications that usually improve after its discontinuation. Possible underlying mechanisms for these complications are discussed. The early diagnosis of these complications may be vital and IFN should be immediately discontinued when early signs of these complications become evident.

[Ulcers on the legs and feet: a seldom recognised side effect of hydroxyurea]. / Ulcera aan de benen en voeten: een weinig herkende bijwerking van hydroxycarbamide.

Three male patients aged 52, 49 and 74 years who were treated with hydroxyurea for chronic myeloid leukaemia (CML) or essential thrombocytosis developed severely painful ulcers on the lower legs and feet after an interval varying from 4 months to 2.5 years. These ulcers only healed after discontinuation of the drug. This is an adverse effect of hydroxyurea that is not infrequently seen but is difficult to recognise. The precise pathogenesis is still unclear but micro-circulatory disorders and a direct cytostatic effect on the epidermal cells probably play a role. Often, the drug has already been used for several years before the ulcers develop. They are resistant to treatment unless the hydroxyurea is stopped. Alternatives to hydroxyurea are imatinib for the treatment of CML and interferon alpha-2a or anagrelide for essential thrombocytosis.

[Bilateral ankle ulcers associated with hydroxyurea therapy for chronic myelogenous leukemia].

Bilateral ankle skin ulcers developed in a 61-year-old man in the chronic phase of chronic myelogenous leukemia receiving hydroxyurea therapy. The circulating immune complex (anti-C3d antibody) was high in this case, but vasculitis was not observed in the pathological findings of biopsied skin materials. This association has been reported in patients who had chronic myelogenous leukemia or other myeloproliferative disorders and were treated with hydroxyurea. It is likely that skin ulcers are caused by hydroxyurea.

[A lower-leg ulcer during hydroxyurea therapy for essential thrombocythemia].

A skin ulcer of the lateral malleous developed in a 61-year-old man receiving hydroxyurea for essential thrombocythemia. In the past, skin ulcers have been reported in patients with chronic myeloproliferative diseases, including essential thrombocythemia, who had been treated with hydroxyurea. In the current case, vasculitis or thrombi in vessels of the biopsied specimen of the lower leg were not observed, and the patient required skin-graft operation. Accordingly, we concluded that the skin ulcer might be due to the administration of hydroxyurea. Thus, the dose of hydroxyurea was decreased.

Late development of Nicolau syndrome: case report.

Nicolau syndrome also known as Embolia cutis medicamentosa and Livedoid dermatitis is a rare complication characterized by tissue necrosis that occurs after injection of medicines. We describe a case of late development of Nicolau syndrome following intra-articular infiltration with corticosteroid.

Síndrome de Nicolau de desenvolvimento tardio: relato de caso / Late development of Nicolau syndrome: case report

A Síndrome de Nicolau, também conhecida como Embolia Cutis Medicamentosa e Dermatite Livedóide, é uma rara complicação caracterizada por necrose tecidual que ocorre após a injeção de medicamentos. Descrevemos um caso de Síndrome de Nicolau de curso tardio, posterior à infiltração intra-articular com corticóide.

Nicolau syndrome also known as Embolia cutis medicamentosa and Livedoid dermatitis is a rare complication characterized by tissue necrosis that occurs after injection of medicines. We describe a case of late development of Nicolau syndrome following intra-articular infiltration with corticosteroid.

Hydroxyurea-related ankle ulcers in patients with myeloproliferative disorders: a case report and review of the literature.

The association of ankle ulcer development with hydroxyurea therapy in patients with myeloproliferative disorders has been reported in two small case series and two patient reports. It is thought that hydroxyurea, an antineoplastic agent with selective cytotoxicity for cells that divide most actively (such as those of the skin), causes these ulcerations through impairment of normal wound healing in areas of common trauma. Treatment modalities reported include discontinuation of medication, debridement, and topical antibiotics. We report the successful split-thickness skin grafting of a hydroxyurea-related ankle ulceration after preoperative discontinuation of hydroxyurea treatment in a patient with chronic myelogenous leukemia who had previously failed grafting while taking this medication. It is hoped that heightened awareness of the link between hydroxyurea and chronic, debilitating ankle ulcerations in patients with myeloproliferative disorders, as well as familiarity with reported treatments, will promote early diagnosis and aggressive management of these unique and relatively uncommon lesions.

A case of bilateral heel ulcers associated with hydroxyurea therapy for chronic myelogenous leukemia.

Bilateral heel skin ulcers developed in a 50-year-old male in the chronic phase of chronic myelogenous leukemia who had been receiving hydroxyurea (HU) therapy for 3 years. Histological examination showed perivascular lymphocytic inflammation without vasculitis. After interruption of HU administration, the heel ulcers were completely resolved within 2 months. The clinical course strongly suggested that the heel ulcers were induced by long-term HU therapy.

Aggressive, extensive, vasculitic leg ulceration associated with hydroxyurea therapy and a fatal outcome.

The association of lower leg ulcer development and hydroxyurea therapy in patients with myeloproliferative disorders has been reported previously. In most of these cases the ulcers healed with cessation of the hydroxyurea together with meticulous attention to wound care. We report a patient who developed painful vasculitic ulcers secondary to hydroxyurea on both lower legs whilst on long-term hydroxyurea therapy for idiopathic thrombocytosis. The ulcers extended relentlessly despite stopping hydroxyurea, maximizing topical therapies and starting intensive systemic treatment. We discuss the association of hydroxyurea therapy with the development of painful ulceration.